Gene Context Sentence
Table 2. Analysis of context sentence of FH gene in 5 abstracts.
|PMID||Gene Context Sentence|
|32389859||Individuals with Familial Hypercholesterolaemia (FH) are at very high risk of cardiovascular disease, which is associated with poor outcomes from coronavirus infections. […] COVID-19 puts strain on healthcare systems and may impair access to routine FH services. […] On behalf of the International Lipid Expert Panel (ILEP) and the European FH Patient Network (FH Europe), we present brief recommendations on the management of adult patients with FH during the COVID-19 pandemic. […] We discuss the implications of COVID-19 infections for FH patients, the importance of continuing lipid-lowering therapy where possible, issues relating to safety monitoring and service delivery.|
|32870376||Statins are first-line therapy for lowering low-density lipoprotein (LDL) cholesterol in familial hypercholesterolemia (FH), particularly in heterozygous patients. […] We review advances and new questions on the use of statins in FH. […] Cumulative evidence from registry data and sub-analyses of clinical trials mandates the value of statin therapy for prevention of atherosclerotic cardiovascular disease (ASCVD) in FH. […] Statins are safe in children and adolescents with FH, with longer term cardiovascular benefits. […] There is no rationale for discontinuation of statins in elderly FH unless indicated by adverse events. […] FH is undertreated, with > 80% of statin-treated FH patients failing to attain LDL cholesterol treatment targets. […] Whether statin use could improve the clinical course of FH patients with COVID-19 and other respiratory infections remains an unsolved issue for future research. […] Statins are the mainstay for primary and secondary prevention of ASCVD in FH. […] Despite their widespread use, statins merit further investigation in FH.|
|33189452||Previous evidence has shown the presence of early endothelial dysfunction in healthy subjects but with a family history of type 2 diabetes (FH-DM2), where glucose metabolism, the synthesis of nitric oxide (NO), reactive oxygen species (ROS), as well as expression of genes involved with their synthesis are impaired. […] Besides, in subjects with an FH-DM2, the presence of hyperinsulinemia and high glucose levels are common events that could favor the infection of endothelial cells by the coronavirus. […] Therefore, we hypothesized that an FH-DM2 should be considered an important risk factor, since the individuals with this background develop an early endothelial dysfunction, which would increase the susceptibility and severity of infection and damage to the endothelium, in the patient infected with the SARS-CoV-2.|
|33540179||Patients with familial hypercholesterolemia (FH) are likely at increased risk for COVID-19 complications in the acute phase of the infection, and for a long time thereafter. […] Because in FH patients the level of low density lipoprotein cholesterol (LDL-C) is elevated from birth and it correlates with the degree of systemic endothelial dysfunction, both heterozygous FH (HeFH) patients and, in particular, homozygous FH (HoFH) patients have a dysfunctional endothelium prone to further damage by the direct viral attack and the hyper-inflammatory reaction typical of severe COVID-19. […] In FH patients, the focus should therefore be on the effective lowering of LDL-C levels, the root cause of the expected excess vulnerability to COVID-19 infection in these patients. […] For the reduction of the excess risk in FH patients with COVID-19, we advocate stringent adherence to the guideline determined LDL-C levels for FH patients, or maybe even to lower levels. […] Unfortunately, epidemiologic data are lacking on the severity of COVID-19 infections, as well as the number of acute cardiac events that have occurred in FH subjects during the COVID-19 pandemic. […] Such data need to be urgently gathered to learn how much the risk for, and the severity of COVID-19 in FH are increased.|
|33564481||Although it is still largely unclear, HBV0-activated sudden-onset strong cytotoxic T lymphocyte response and enhanced viral replication and/or retention of the viral capsid in infected hepatocytes may cause the pathogenesis of FH.|